Evidence map›Paper›PMID 28212753›Full record

ArticleMolecular cell2017

The TRAIL-Induced Cancer Secretome Promotes a Tumor-Supportive Immune Microenvironment via CCR2.

Torsten Hartwig, Antonella Montinaro, Silvia von Karstedt, Alexandra Sevko, Silvia Surinova, Ankur Chakravarthy, Lucia Taraborrelli, Peter Draber, Elodie Lafont, Frederick Arce Vargas and 3 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07511062 (Axatilimab Combined With Decitabine/Venetoclax for the Treatment of TP53-mutated/Deleted AML Patients), which is not on this map. Cited by 157 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 2 pooled it
9.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07511062 phase1not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Axatilimab Combined With Decitabine/Venetoclax for the Treatment of TP53-mutated/Deleted AML Patients

TypeinterventionalSponsorNorthside Hospital, Inc.Ran2026 to 2030Enrolled32ConditionsAcute Myeloid Leukemia, TP53 Gene MutationArmsDecitabine, Venetoclax, Axatilimab
3 · Its place in the literature

Who cites it

157 citing papers in PubMed, 2 syntheses or guidelines pooled it, 240 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026
    Review
  11. Review
  12. An atlas of ferroptosis-induced secretomes.Cell death and differentiation · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

97 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Torsten HartwigCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Antonella MontinaroCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Silvia von KarstedtCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Alexandra SevkoCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Silvia SurinovaCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Ankur ChakravarthyDepartment of Oncology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Lucia TaraborrelliCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Peter DraberCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Elodie LafontCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Frederick Arce VargasCancer Immunology Unit, Department of Haematology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Mona A El-BahrawyDepartment of Histopathology, Imperial College London, London W12 0NN, UK.
Sergio A QuezadaCancer Immunology Unit, Department of Haematology, UCL Cancer Institute, University College London, London WC1E 6DD, UK.
Henning WalczakCentre for Cell Death, Cancer, and Inflammation, Department of Cancer Biology, UCL Cancer Institute, University College London, London WC1E 6DD, UK. Electronic address: h.walczak@ucl.ac.uk.
University College London · GBCRUK Lung Cancer Centre of Excellence · GBImperial College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/I004580/1Cancer Research UK 10950Cancer Research UK 17341Cancer Research UK 20265Cancer Research UK 22246Wellcome Trust
6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known for specifically killing cancer cells, whereas in resistant cancers, TRAIL/TRAIL-R can promote metastasis via Rac1 and PI3K. It remains unknown, however, whether and to what extent TRAIL/TRAIL-R signaling in cancer cells can affect the immune microenvironment. Here we show that TRAIL-triggered cytokine secretion from TRAIL-resistant cancer cells is FADD dependent and identify the TRAIL-induced secretome to drive monocyte polarization to myeloid-derived suppressor cells (MDSCs) and M2-like macrophages. TRAIL-R suppression in tumor cells impaired CCL2 production and diminished both lung MDSC presence and tumor growth. In accordance, the receptor of CCL2, CCR2, is required to facilitate increased MDSC presence and tumor growth. Finally, TRAIL and CCL2 are co-regulated with MDSC/M2 markers in lung adenocarcinoma patients. Collectively, endogenous TRAIL/TRAIL-R-mediated CCL2 secretion promotes accumulation of tumor-supportive immune cells in the cancer microenvironment, thereby revealing a tumor-supportive immune-modulatory role of the TRAIL/TRAIL-R system in cancer biology.

Indexed as

Tumor MicroenvironmentA549 CellsAdenocarcinomaAdenocarcinoma of LungAnimalsCarcinoma, Non-Small-Cell LungCaspase 8Cell ProliferationChemokine CCL2CytokinesFas-Associated Death Domain ProteinFemaleHCT116 CellsHeLa CellsHumansLung NeoplasmsCASP8 protein, humanCaspase 8CCL2 protein, humanCCR2 protein, humanChemokine CCL2CytokinesFADD protein, humanFas-Associated Death Domain ProteinReceptors, CCR2Receptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanCCL2CCR2cytokineFADDMDSCmicroenvironmentTRAILTRAIL-Rtumor

Identifiers

PMID28212753
PMCPMC5316415
OpenAlexW2588975115

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.